Endothelial Dysfunction and Subendothelial Monocyte Macrophages in Hypertension: Effect of Angiotensin Converting Enzyme Inhibition
Hypertension is associated with an impairment of endothelium-dependent relaxation. The angiotensin converting enzyme inhibitors captopril and cilazapril can prevent this endothelial dysfunction. We recently observed that long-term treatment with cilazapril could also prevent subendothelial infiltrat...
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Published in | Hypertension (Dallas, Tex. 1979) Vol. 18; no. 2; pp. 132 - 141 |
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Main Authors | , , , |
Format | Journal Article |
Language | English |
Published |
Philadelphia, PA
American Heart Association, Inc
01.08.1991
Hagerstown, MD Lippincott |
Subjects | |
Online Access | Get full text |
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Abstract | Hypertension is associated with an impairment of endothelium-dependent relaxation. The angiotensin converting enzyme inhibitors captopril and cilazapril can prevent this endothelial dysfunction. We recently observed that long-term treatment with cilazapril could also prevent subendothelial infiltration by mononuclear cells in spontaneously hypertensive rats. This prompted us to examine whether, in spontaneously hypertensive rats, endothelial dysfunction and subendothelial infiltration by mononuclear cells are associated. These cells were characterized as monocyte macrophages. Infiltration by monocyte macrophages was quantified by morphometry. Endothelial function was estimated by calculating serotonin ratio (maximal contraction to serotonin on isolated arterial rings with endothelium over maximal contraction on paired rings without endothelium). The regional distribution of endothelial dysfunction and subendothelial monocyte macrophages was similar. Both were maximal in the carotid artery, less in the aorta, and nonexistent in the renal artery. A 2-week treatment with cilazapril decreased both endothelial dysfunction (serotonin ratio decreased by 32%) and the number of subendothelial monocyte macrophages in the aorta, which decreased by 38%. We conclude that in spontaneously hypertensive rats, endothelial dysfunction and subendothelial monocyte macrophage infiltration are associated and that cilazapril can decrease both. The observation that angiotensin converting enzyme inhibitors affect subendothelial accumulation of monocyte macrophages may lead to a better understanding of the mechanism of action of this class of drugs. |
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AbstractList | Hypertension is associated with an impairment of endothelium-dependent relaxation. The angiotensin converting enzyme inhibitors captopril and cilazapril can prevent this endothelial dysfunction. We recently observed that long-term treatment with cilazapril could also prevent subendothelial infiltration by mononuclear cells in spontaneously hypertensive rats. This prompted us to examine whether, in spontaneously hypertensive rats, endothelial dysfunction and subendothelial infiltration by mononuclear cells are associated. These cells were characterized as monocyte macrophages. Infiltration by monocyte macrophages was quantified by morphometry. Endothelial function was estimated by calculating serotonin ratio (maximal contraction to serotonin on isolated arterial rings with endothelium over maximal contraction on paired rings without endothelium). The regional distribution of endothelial dysfunction and subendothelial monocyte macrophages was similar. Both were maximal in the carotid artery, less in the aorta, and nonexistent in the renal artery. A 2-week treatment with cilazapril decreased both endothelial dysfunction (serotonin ratio decreased by 32%) and the number of subendothelial monocyte macrophages in the aorta, which decreased by 38%. We conclude that in spontaneously hypertensive rats, endothelial dysfunction and subendothelial monocyte macrophage infiltration are associated and that cilazapril can decrease both. The observation that angiotensin converting enzyme inhibitors affect subendothelial accumulation of monocyte macrophage may lead to a better understanding of the mechanism of action of this class of drugs. Hypertension is associated with an impairment of endothelium-dependent relaxation. The angiotensin converting enzyme inhibitors captopril and cilazapril can prevent this endothelial dysfunction. We recently observed that long-term treatment with cilazapril could also prevent subendothelial infiltration by mononuclear cells in spontaneously hypertensive rats. This prompted us to examine whether, in spontaneously hypertensive rats, endothelial dysfunction and subendothelial infiltration by mononuclear cells are associated. These cells were characterized as monocyte macrophages. Infiltration by monocyte macrophages was quantified by morphometry. Endothelial function was estimated by calculating serotonin ratio (maximal contraction to serotonin on isolated arterial rings with endothelium over maximal contraction on paired rings without endothelium). The regional distribution of endothelial dysfunction and subendothelial monocyte macrophages was similar. Both were maximal in the carotid artery, less in the aorta, and nonexistent in the renal artery. A 2-week treatment with cilazapril decreased both endothelial dysfunction (serotonin ratio decreased by 32%) and the number of subendothelial monocyte macrophages in the aorta, which decreased by 38%. We conclude that in spontaneously hypertensive rats, endothelial dysfunction and subendothelial monocyte macrophage infiltration are associated and that cilazapril can decrease both. The observation that angiotensin converting enzyme inhibitors affect subendothelial accumulation of monocyte macrophages may lead to a better understanding of the mechanism of action of this class of drugs. |
Author | Baumgartner, Hans R Clozel, Martine Kuhn, Herbert Hefti, Fridolin |
AuthorAffiliation | Pharmaceutical Research Department, F. Hoffmann-La Roche Ltd, Basel, Switzerland |
AuthorAffiliation_xml | – name: Pharmaceutical Research Department, F. Hoffmann-La Roche Ltd, Basel, Switzerland |
Author_xml | – sequence: 1 givenname: Martine surname: Clozel fullname: Clozel, Martine organization: Pharmaceutical Research Department, F. Hoffmann-La Roche Ltd, Basel, Switzerland – sequence: 2 givenname: Herbert surname: Kuhn fullname: Kuhn, Herbert – sequence: 3 givenname: Fridolin surname: Hefti fullname: Hefti, Fridolin – sequence: 4 givenname: Hans surname: Baumgartner middlename: R fullname: Baumgartner, Hans R |
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SubjectTerms | Acetylcholine - pharmacology Angiotensin-Converting Enzyme Inhibitors - pharmacology Animals Antihypertensive agents Aorta - drug effects Aorta - pathology Biological and medical sciences Captopril - pharmacology Cardiovascular system Carotid Arteries - drug effects Carotid Arteries - pathology Cell Movement - drug effects Cilazapril Dose-Response Relationship, Drug Endothelium, Vascular - pathology Endothelium, Vascular - physiopathology Hypertension - drug therapy Hypertension - physiopathology Macrophages - physiology Male Medical sciences Norepinephrine - pharmacology Peptidyl-Dipeptidase A - physiology Pharmacology. Drug treatments Pyridazines - pharmacology Rats Rats, Inbred SHR Rats, Inbred WKY Renal Artery - drug effects Renal Artery - pathology Serotonin - pharmacology Vasoconstriction - drug effects Vasodilation - drug effects |
Title | Endothelial Dysfunction and Subendothelial Monocyte Macrophages in Hypertension: Effect of Angiotensin Converting Enzyme Inhibition |
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